1. Field of the Invention
This invention pertains generally to a self-organizing electrode stimulation network, and more particularly to a self-organizing electrode stimulation network and methods for cardiac resynchronization therapy.
2. Description of Related Art
When the heart as a pump is unable to meet the needs of the body, heart failure (HF) is said to be present. HF is a major cause of morbidity and mortality in the developed countries, and has an important impact on economic productivity, as it leads to substantial absenteeism and hospitalizations. About 5 million people in this country have HF, and over half a million are diagnosed with HF each year! It is the primary reason for 12 to 15 million office visits to health care providers each year, and it accounts for over 6 million hospital days/year. HF is the single most common reason for hospitalization in the Medicare database (composed principally of patients over the age of 65 years), and Medicare spends more dollars on HF management than on any other diagnosis. The prevalence of HF in the population has increased over time, especially in the elderly and truly elderly (>85 years) groups.
HF may result from a failure of the contractile pumping action of the heart (systolic HF), or conversely by an inability of the heart to fill with blood normally despite preserved contractile function (diastolic HF). While both forms of HF may be devastating in their manifestations, systolic HF has, until recently, attracted substantially more interest; perhaps as a consequence, there is now good evidenced-based data to support the use of specific pharmacologic therapies to improve not only symptoms but also morbidity and mortality due to systolic HF.
Standard pharmacologic therapy for heart failure has become standard place over the last several decades. Beta adrenergic blockers, angiotension converting enzyme inhibitors and/or angiotension receptor blockers, aldosterone antagonists, loop diuretics, and digoxin in some settings have been shown to ameliorate symptoms and/or reduce mortality in HF. The risk of death has also been reduced by the implantation of an internal cardioverter defibrillator (LCD) in appropriate candidates. Yet, despite optimal medical therapy, some patients remain symptomatic, a few of the end-stage patients are fortunate to undergo cardiac transplantation.
A promising avenue for patients who are not candidates for heart transplantation is cardiac resynchronization therapy (CRT). After FDA approval in 2001, a steady growth has occurred in cardiac resynchronization therapy (CRT) for the treatment of heart failure. As early as 2004, over 40,000 units were implanted in the U.S. alone with growth predicted for the future.
CRT uses a special pacemaker to improve the pumping action of the heart. When the heart becomes damaged and its pumping function impaired, the pumping chambers may contract in an uncoordinated and dyssynchronous manner that is inefficient and generally ineffective.
It has been shown that if both the right and left ventricles are paced simultaneously, the amount of uncoordinated pumping action is reduced, and the output from the left ventricle improves. Previously, the only way to deliver the requisite electric stimulation to “resynchronize” the heart was by the use of a specially configured pacemaker that was implanted under the skin using time-honored pacemaker techniques.
Using existing methods, two pacing leads are commonly attached using hard-wired connections to the pacemaker generator box, one positioned in the right and the other in the left ventricle (actually, the left ventricular lead is placed in a cardiac vein that runs on the surface of the heart, but biventricular pacing is achieved nonetheless). However, approximately 50% of patients do not respond to this approach, due to damages in the muscle tissue of the heart which create uneven or dyssynchronous pumping conditions (mechanical dys-synchrony), or which prevent electrical (pacing) signals from traveling through the muscle tissue to the proper location.
It is believed that existing CRT methods do not effectively depolarize regions of contractile myocardial tissue that are electrically isolated, and are not effective if different regions of the myocardium need to be sequentially depolarized at different times for an effective contraction to occur.
While the reasons for non-response have many factors, multiple endocardial pacing electrodes may be able to normalize nearly any derangements of dys-synchronous contraction. Thus, more pacing sites may result in effective therapy for some of these non-responders.
However, existing CRT methods require the use of leads to electrically connect the electrodes to the central control, which limits the number of electrodes implanted. Also existing CRT methods require the use of an implanted case with a battery. Furthermore, placing more leads in the heart can cause complications such as blood clots, altered flow patterns, and higher probability of lead mechanical failure. These complications become more critical in pediatric patients due to smaller heart anatomy.
Accordingly, an object of the present invention is a self-organizing system and means for stimulating multiple locations in a biological tissue (such as a heart muscle) which can coordinate the timing of the stimulation at these multiple locations separately in order to optimize the desired performance or condition of the biological tissue. Another object is a real-time system for evaluating ventricular contractility in a safe, effective, and reproducible way to restore ventricular function. At least some of these objectives will be met in the description provided below.